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Pathophysiology > Ch. 33 Diabetes Mellitus > Flashcards

Ch. 33 Diabetes Mellitus Flashcards

1
Q

What is the definition of diabetes mellitus?

A

A disorder of carbohydrate, fat, and protein metabolism resulting from lack of insulin availability or lack of effectiveness.

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2
Q

What are the four types of diabetes?

A

Type I

Type II

Gestational (GDM)

Other

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3
Q

What is type I diabetes?

A

`AUTOIMMUNE: destruction of the beta cells and absolute insulin deficiency

tends to happen earlier in life

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4
Q

What is type II diabetes?

A

INSULIN RESISTANCE: as well as a relative insulin deficiency; an adaptive response to over nutrition

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5
Q

What is gestational diabetes?

A

glucose intolerance detected first during pregnancy

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6
Q

What are some “other” diabetes?

A

diabetes associated with other conditions:

most often pancreatic diseases or endocrine disorders

SOME TEMPORARY, SOME PERMANENT

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7
Q

What are normal lab values for someone without diabetes?

A

FPG (fasting plasma glucose):

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8
Q

What are the lab values for someone who is impaired fasting plasma glucose/ impaired glucose tolerance (pre-diabetes)?

A

FPG (fasting plasma glucose): 100-125 mg/dl

OGGTT (oral glucose tolerance test): 140-199 mg/dl

A1C: 5.7%-6.4%

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9
Q

What are the lab values for someone with diabetes (REGARDLESS OF THE TYPE)?

A

FPG (fasting plasma glucose): >125 mg/dl (2 or more occasions)

OGGTT (oral glucose tolerance test): >200 mg/dl

A1C: >6.5%

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10
Q

What is the best test to use for checking average blood sugar?

A

A1C - once the glucose is in the RBC it doesnt get out until the cell dies

MAKES IT HARD FOR SOMEONE TO FAKE A GOOD TEST RESULT

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11
Q

Would you do an OGGTT for someone you know has glucose tolerance issues?

A

Not normally, usually this test is done for suspected gestational diabetes cases

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12
Q

How many people with type I diabetes have the autoimmune version?

A

95%

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13
Q

What brings on type IA diabetes?

A

Genetic predisposition

environmental trigger

t lymphocyte mediated hypersensitivity reaction to beta cell (autoantibodies)

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14
Q

What cells are destroyed in type IA diabetes?

A

the beta cells

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15
Q

What are people with type I diabetes prone to?

A

ketoacidosis (insulin helps stop lipolysis)

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16
Q

When does type I generally develop?

A

younger people, but can occur at any age

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17
Q

What is the honeymoon period of type I diabetes?

A

this is a time during early diagnosis where it seems like the beta cells regenerate and the symptoms disappear

VERY SHORT PERIOD OF TIME

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18
Q

If we came up with an immune modification treatment, when would it be most effective?

A

If we caught it early, so the pancreas would still have some beta cells left to produce insulin.

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19
Q

What type of diabetes do 90-95% of people with diabetes have?

A

type II

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20
Q

What defines type II diabetes?

A

fasting hyperglycemia even with the availability of insulin

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21
Q

What are the mechanisms of type II diabetes?

A

peripheral insulin resistance (inefficient receptors on target cells)

deranged beta cell secretion of insulin

increased hepatic glucose production

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22
Q

Can beta cells get worn out from secreting too much insulin with type II diabetes?

A

YES, the body will keep telling the beta cells to make insulin because their sugars wont go down, even when the insulin levels are high

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23
Q

What other metabolic abnormalities does hyperglycemia contribute to?

A

elevated triglycerides, low HDL, hypertension, abnormal fibrinolysis, coronary artery disease

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24
Q

What are some risk factors for type II diabetes?

A

family history, obesity, physical inactivity, fat distribution (weight carrying in upper body and trunk)

MOST PEOPLE WITH DISEASE HAVE A GENETIC PREDISPOSITION FOR IT AS WELL

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25
Q

What do chronic high FFA (free fatty acid levels) with obesity lead to?

A

beta cell dysfunction

tissue insulin resistance

reduced hepatic insulin sensitivity

triglyceride accumulation in the liver

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26
Q

What does obesity do to our resistance to the action of insulin and the livers production of glucose?

A

Increases our insulin resistance and liver production of glucose. (causes hyperglycemia and hyperinsulinemia)

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27
Q

Can insulin resistance improve with weight loss?

A

YES YES YES

just eating less and losing weight can help

BUT

weight loss is even better if coupled with exercise

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28
Q

How would exercise help with diabetes?

A

It helps the muscles take in more glucose

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29
Q

What are the requirements that you have to have at least three of to be considered to have metabolic syndrome? (there are 5)

A

Increased FPG: >100 mg/dl

Abdominal obesity: waist circumference >35” in women and >40” in men

increased blood triglyceride levels: greater than or equal to 150

decreased HDL levels: 130/85 mm Hg

COMMON IN PEOPLE WITH TYPE II DIABETES

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30
Q

What are some other things you might see in someone with metabolic syndrome (harder to initially assess)?

A

systemic inflammation

elevated C reactive protein level (high risk for cardiac events)

abnormal fibrinolysis

abnormal functioning of vascular endothelium (Higher risk for clots)

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31
Q

What are some causes of “other” specific types of diabetes (secondary diabetes)?

A

Pancreatic disease

cushings syndrome

acromegaly

pheochromocytoma

medications:

    • loop and thiazide diuretics (watch when treating diabetic with hypertension)
    • glucocorticoids
    • oral contraceptives
    • anti-psychotics

IF THESE DISEASES ARE REVERSED OR MEDS ARE STOPPED THE DIABETES WILL MORE THAN LIKELY GO AWAY

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32
Q

What is the definition of gestational diabetes?

A

glucose intolerance first detected during pregnancy

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33
Q

What are women with GDM (gestational diabetes mellitus) at high risk for?

A

complications with pregnancy

mortality

fetal abnormalities

developing type II diabetes 5-10 years after delivery

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34
Q

What are some risk factors for GDM?

A

family history of diabetes

obesity

glycosuria
history of stillbirth or spontaneous abortion

fetal abnormalities in previous pregnancy

previous large or heavy-for-date infant

of advanced maternal age (over 25)

five or more pregnancies

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35
Q

When do we do a OGGTT to check for gestational diabetes during pregnancy?

A

24-28 weeks

THEORETICALLY DONE FOR HIGH RISK POPULATION, BUT MOST EVERY PREGNANT WOMEN GETS SCREENED FOR THIS

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36
Q

What are some of the diagnostic methods for checking blood glucose?

A

FBG (fasting blood glucose)

casual (random) blood glucose

glucose tolerance test

glycosated hemoglobin (HbA1C)

urine tests

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37
Q

What is an FBG?

A

these are glucose levels measured after being with held from food for 8-12 hours

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38
Q

What is a casual (random) blood glucose, and what is considered diabetic?

A

done with no regard to meal times of that day

elevated glucose (>200 mg/dl) with the presence of classic DM symptoms:

    • polydispia
    • polyphagia
    • polyuria
    • blurred vision
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39
Q

What is a glucose tolerance test?

What is the normal outcome?

Abnormal?

A

measures the bodies ability to store glucose by removing it from the blood

normally BG levels will return to normal after 2-3 hours after ingestion of glucose (this means there is sufficient insulin present to remove it from the blood into the cells)

If the glucose levels stay elevated for a long period of time

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40
Q

What is HbA1c? (glycosated hemoglobin)

Why is this a great tool?

What does the ADA say is the level that needs intervention?

A

Measure the amount hemoglobin that has glucose incorporated into it

entry of glucose into RBC is not insulin dependent, it is dependent on the BG levels of the blood, and is not reversible

This tells us an index of what the BG levels have been during the last 2-3 months

greater than 7% needs corrective measures

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41
Q

What is the urine test?

Who will mainly get this test?

A

This is a test for ketones in the urine

mainly for type I diabetics or those prone to ketoacidosis… but not common test for anything else because home BG tests have become so accurate

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42
Q

Do type I diabetics always need interventions for blood sugar regulation?

A

YES, they always need to put insulin into their body

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43
Q

What antidiabetic medications do type II diabetics need?

A

They can take oral medications if caught early enough, but they will eventually need insulin

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44
Q

What is a general view about the proper diet for type I and II diabetics?

A

type I: monitor their food intake so insulin can be adjusted properly

Type II: weight loss diet

45
Q

What about exercise and type I and II diabetics?

A

type I: exercise for its general benefits

type II: need to exercise for weight loss

Both: enhances peripheral insulin reception and can lead to hypoglycemia

THE EXERCISE NEEDS TO BE REGULAR, NOT SPORADIC, THIS HELPS SCHEDULE INSULIN ADMINISTRATION SCHEDULE

46
Q

What is happening in the body of people with type II diabetes?

A

impaired insulin secretion/excessive glucagon secretion

carbohydrate absorption (typically high because of obesity)

decrease insulin-stimulated glucose uptake

increased basal hepatic glucose production

47
Q

What are the major effects and minor effects of the biguanides for type II DM?

A

Major: decrease hepatic glucose output

Minor: increases peripheral glucose uptake

48
Q

What are the minor and major effects of thiazolidinediones for type II DM?

A

major: increase peripheral uptake of glucose
minor: decrease hepatic glucose output

49
Q

What is the major effect of glucosidase inhibitors and amylin analogs for type II diabetes?

A

decrease glucose absorption in intestines

AMYLIN ANALOGS ALSO DECREASE GLUCAGON SECRETION

often causes diarrhea and other GI effects

50
Q

What are the major effects of insulin secretagogues incretins for type II diabetes?

A

increase insulin secretion and decrease glucagon secretion

51
Q

Can type I diabetics take oral medications for their disease?

A

NO, their beta cells dont function at all

52
Q

Is it true that a type II diabetics pancreas will eventually burn out and require them to go to insulin injections?

A

YES YES YES

often oral meds alone are sufficient for 5 years when caught early

53
Q

What are the different types of insulin we use for injections?

A

short acting (regular)

Rapid acting (lispro, aspart, glulisine)

Long acting (NPH, glargine, determir)

54
Q

How long is the onset and duration for short acting insulin?

A

onset: 30 minutes
duration: 5-8 hours

55
Q

What is the onset for rapid acting insulin?

A
56
Q

What is the onset and duration for long acting insulin?

A

onset: several hours
duration: 12-24 hours

CAN BE SPLIT UP INTO INTERMEDIATE AND LONG ACTING

57
Q

Do people usually have multiple insulin injections a day?

A

YES

best if its a combination of intermediate and immediate (rapid) acting

58
Q

What if a patient isnt compliant with having a lot of insulin injections a day?

A

will have to do less frequent shots of long acting insulin

doesnt work quite as well

59
Q

What is another way to get insulin into the body?

A

A continuous subcutaneous insulin infusion pump

60
Q

What are kids especially at high risk for?

A

very low blood sugars

can cause cognitive damage, which can be permanent if they have many hypoglycemic episodes

61
Q

What does the fact that kids BG tends to run low a lot do for our treatment?

A

we tend to let them run a little higher when it comes to BG levels

62
Q

What do we look at when choosing route and method of insulin to go with?

A

diet

lifestyle

ability to comply

63
Q

What are some acute complications with hyperglycemia?

A

Diabetic ketoacidosis (DKA)

Hyperosmolar Hyperglycemic State (HHS)

64
Q

With what type of diabetes is DKA more common?

A

Type I

65
Q

What are the mechanisms of DKA?

A

LACK OF INSULIN

this results in the breakdown of tryglycerides into fatty acids and glycerol that, causes an increase in production of ketones by the liver when the fatty acids are used for energy

66
Q

With what type of DM is HHS (hyperosmolar hyperglycemicc state) more common?

A

type II

67
Q

What is the mechanism of HHS (hyperosmolar hyperglyccemic state)?

A

Elevated serum glucose levels due to and increased intake of carbohydrates or an increased resistance to insulin

USUALLY HAVE JUST ENOUGH INSULIN PRESENT TO PREVENT KETONE PRODUCTION

68
Q

What are the three major derangements that make a definitive diagnosis of DKA?

A

Hyperglycemia >250 mg/dl

ketosis (ketonemia at 1:2 dilution and ketonuria)

metabolic acidosis (low bicarb

69
Q

What are the clinical presentations of diabetic ketoacidosis?

A

slow onset; prolonged recovery

1-2 days of polyuria, polydispia, nausea, vomiting, marked fatigue: may progress to stupor or coma

fruity breath because of volatile ketoacids being blown off with CO2

abdominal tenderness and hypotension

compensatory mechanisms: tachycardia and tachypnea

high levels of counterregulatory hormones

70
Q

What is the problem with DKA and the presence of counterregulatory hormones?

A

These hormones are trying to raise our BG even more, this makes up have to treat the whole process, usually we give low dose insulin to slowly lower BG and keep it steadily lowered to not trigger the release of these counterregulatory hormones

71
Q

What can hyperglycemia lead to?

A

polyuria

dehydration

critical loss of electrolytes (can be cause of neurologic symptoms)

72
Q

What does hyperglycemia do to the ECF and ICF?

A

The ECF is hyperosmolar which causes a water and potassium shift from ICF to ECF

73
Q

What about hyperglycemia and triglycerides one more time?

A

the lack of insulin lead to the breakdown of triglycerides to fatty acids and glycerol, which when used for energy increases ketone production by the liver

74
Q

What do the excess ketoacids cause?

A

metabolic acidosis, this causes a decrease in serum bicarb levels

BUFFER SYSTEM CAN BE INHIBITED SOMEWHAT BY SHIFT OF POTASSIUM OUT OF CELLS

75
Q

Is the onset of HHS rapid?

A

NO

it is insidious

76
Q

With what age group does HHS most often occur?

A

elderly

often mistaken for a stroke because of neurological manifestations

77
Q

What characterizes HHS?

A

Hyperglycemia >600 mg/dl

hyperosmolarity >320 mOsm/L (pulls water from cells which causes dehydration, excessive thirst, neurological signs and symptomssuch as seizures, hemiparesis, aphasia, visual disturbances

absence of ketoacids

decreased LOC

78
Q

What are the factors that contribute to HHS?

A

increased resistance to the effect of insulin

excessive carbohydrate intake

79
Q

What causes hyperglycemia?

A

too much food

too little insulin

illness or stress

80
Q

What is the onset of hyperglycemia?

A

gradual, can progress to coma

81
Q

What are the blood sugar levels for hyperglycemia?

A

above 200 mg/dl

82
Q

What is the normal blood sugar range?

A

70-115 mg/dl

83
Q

What do you do if your blood sugar is over 250 mg/dl for several tests?

A

call the doctor

84
Q

What are the symptoms of hyperglycemia?

A

polydispia

polyuria

dry skin

polyphagia

blurred vision

drowsiness

nausea

85
Q

What is hypoglycemia often referred to as?

A

insulin reaction

86
Q

What are our insulin levels in relation to our glucose levels?

A

insulin levels are excessive and glucose levels are below normal

87
Q

What type of DM does hypoglycemia most often occur?

A

Type I

88
Q

What are some precipitating factors for hypoglycemia?

A

insulin dosage error

failure to eat

increased exercise or random exercise

decreased need of insulin after removal of stress

medication dosage changes

alcohol decreases gluconeogenesis and may cause hypoglycemia if consumed in large amounts or on empty stomach

89
Q

What is the onset and progression of hypoglycemia like?

A

rapid, may progress to shock

90
Q

What are the manifestations of hypoglycemia?

A

very wide variation

altered cerebral function

headache

weakness and fatigue

difficulty making decisions

seizures

dizziness

shaking

irritable

behavioral disturbances

coma

PNS = hunger

SNS = anxiety, tachycardia, diaphoresis, vasoconstriction (cool and clammy skin)

91
Q

Do you treat a patient who isnt alert orally?

A

NO NO NO

92
Q

What BG level is considered hypoglycemic?

A
93
Q

What can you do if youre hypoglycemic?

A

drink OJ or milk

eat hard candies

test BG

30 minutes after symptoms go away eat a snack

contact doctor if symptoms dont stop

94
Q

Describe the somogyi effect.

A

These are hyperglycemic episodes that are directly following a hypoglycemic episode

it is said that this is because the body reacts to insulin induced hypoglycemia by using a compensatory mechanism that releases counterregulatory hormones that elevate the serum glucose and may cause some degree of INSULIN RESISTANCE

95
Q

When does the somogyi effect often occur?

A

often at night but can be at random unrecognized times

MAKES IT HARD TO DIAGNOSE

96
Q

What is the dawn phenomenon?

A

an unexplained morning rise in fasting BG levels, believed to be caused by a changce in the normal circadian rhythm for glucose tolerance and an inappropriate increase in counterregulatory hormones

The fasting (pre-breakfast) level is higher than the pre-bedtime (should be higher) level

When this is coupled with the somogyi effectn (often is) there can be a profound increase in BG in the mornings

97
Q

Where do chronic complications of DM most often occur?

A

in insulin independent tissues of the body (dont require insulin for glucose entry into the cell)

98
Q

What is the most important factor for chronic diabetic complications?

A

the chronic glycemic levels of the blood

99
Q

What are the common chronic effects of diabetes?

A

neuropathies

nephropathies

retinopathies

macrovascular complications; cardiovascul disease and stroke

foot ulcers

INFECTIONS

100
Q

What is the pathology of neuropathies?

A

thickening of walls of nutrient vessels that supply nerves

ischemia is ultimately responsible for neural changes

segmental demylenation of schwann cells

101
Q

What are the two types of neuropathy?

A

somatic

autonomic

102
Q

Describe somatic neuropathy

A

diminished perception of vibration, pain, temperature

usually bilaterteral and symmetric

usually in a stocking-glove pattern

increased risk of falling, serious burns, injuries to feet

103
Q

describe autonomic neuropathy.

A

defects in vasomotor responses

    • decreased cardiac responses
    • impaired gastric motility and hypersecretion
    • inability to empty bladder; urinary stasis and UTI
    • sexual dysfunction: leading physiologic cause of sexual dysfunction
104
Q

Describe diabetic nephropathy

A

leading cause of end-stage renal disease

causes lesions that effect glomeruli

early manifestation is microalbuminemia

    • increased protein loss through urine
    • risk increases with A1c levels greater than 8.1%

hypertension accelerates the progression, critical to keep under control

smoking doubles rate of progression of ESRD in type II DM

105
Q

Describe diabetic retinopathies.

A

leading cause of blindness in the US

High lipids, poor glycemic control, hypertension are risk factors

Characteristics:

retinal hemorrhages

abnormal retinal vascular permeability

microaneurysm formation

scarring

retinal detachment

106
Q

Describe the macrovascular complications of DM.

A

High risk for:

    • coronary artery disease
    • stroke
    • peripheral vascular disease

many risks for vascular disease are present in people with diabetes:

    • obesity
    • hypertension
    • hyperglycemia
    • hyperinsulinemia
    • hyperlipidemia
    • altered platelet function
    • elevated fibrinogen levels

RISK FOR PLAGUE BUILDUP THAT CAUSES HARDENING OF THE ARTERIES, CAUSES HYPERTENSION, AGGRAVATES KIDNEY ISSUES, CAUSES IMPAIRED BLOOD FLOW, MAKES IT HARD TO FIGHT INFECTION

107
Q

describe diabetic foot ulcers.

A

distal symmetric neuropathy is a major risk factor for foot ulcers; because you might be unaware of trauma or pain

abnormal focus of pressure + loss of sensation means a foot ulcer may occur

diabetics should have a full foot examination once a year

108
Q

describe the somatosensory testing for diabetics feet.

A

monofilament test:

applies 10g of pressure at the point of contact

4-10 sites are tested for sensation

109
Q

With DKA, if you just treat the hyperglycemia has the complication been fixed?

A

Not necssarily, you would still have to worry about the acidosis.

Pathophysiology (13 decks)

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